Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, PA, USA.
Eur J Neurosci. 2013 Jan;37(2):212-30. doi: 10.1111/ejn.12042. Epub 2012 Nov 4.
The neural mechanisms generating rhythmic bursting activity in the mammalian brainstem, particularly in the pre-Bötzinger complex (pre-BötC), which is involved in respiratory rhythm generation, and in the spinal cord (e.g. locomotor rhythmic activity) that persist after blockade of synaptic inhibition remain poorly understood. Experimental studies in rodent medullary slices containing the pre-BötC identified two mechanisms that could potentially contribute to the generation of rhythmic bursting: one based on the persistent Na(+) current (I(NaP)), and the other involving the voltage-gated Ca(2+) current (I(Ca)) and the Ca(2+) -activated nonspecific cation current (I(CAN)), activated by intracellular Ca(2+) accumulated from extracellular and intracellular sources. However, the involvement and relative roles of these mechanisms in rhythmic bursting are still under debate. In this theoretical/modelling study, we investigated Na(+)-dependent and Ca(2+)-dependent bursting generated in single cells and heterogeneous populations of synaptically interconnected excitatory neurons with I(NaP) and I(Ca) randomly distributed within populations. We analysed the possible roles of network connections, ionotropic and metabotropic synaptic mechanisms, intracellular Ca(2+) release, and the Na(+)/K(+) pump in rhythmic bursting generated under different conditions. We show that a heterogeneous population of excitatory neurons can operate in different oscillatory regimes with bursting dependent on I(NaP) and/or I(CAN), or independent of both. We demonstrate that the operating bursting mechanism may depend on neuronal excitation, synaptic interactions within the network, and the relative expression of particular ionic currents. The existence of multiple oscillatory regimes and their state dependence demonstrated in our models may explain different rhythmic activities observed in the pre-BötC and other brainstem/spinal cord circuits under different experimental conditions.
哺乳动物脑干中产生节律性爆发活动的神经机制,特别是在参与呼吸节律产生的前脑桥(pre-BötC)和脊髓中(例如运动节律性活动),在抑制性突触阻断后仍然知之甚少。在包含 pre-BötC 的啮齿动物延髓切片的实验研究中,确定了两种可能有助于产生节律性爆发的机制:一种基于持续的钠离子电流(I(NaP)),另一种涉及电压门控钙离子电流(I(Ca))和钙离子激活的非特异性阳离子电流(I(CAN)),由细胞外和细胞内来源的细胞内钙离子积累激活。然而,这些机制在节律性爆发中的参与和相对作用仍存在争议。在这项理论/建模研究中,我们研究了具有 I(NaP)和 I(Ca)随机分布的突触连接兴奋性神经元的单个细胞和异质群体中产生的钠依赖性和钙依赖性爆发。我们分析了网络连接、离子型和代谢型突触机制、细胞内钙离子释放以及钠/钾泵在不同条件下产生节律性爆发的可能作用。我们表明,兴奋性神经元的异质群体可以在不同的振荡状态下工作,爆发依赖于 I(NaP)和/或 I(CAN),或者独立于两者。我们证明,工作爆发机制可能取决于神经元兴奋、网络内的突触相互作用以及特定离子电流的相对表达。我们模型中演示的多个振荡状态及其状态依赖性的存在可能解释了在不同实验条件下 pre-BötC 和其他脑干/脊髓回路中观察到的不同节律性活动。